Evacetrapib
Commentary marks evacetrapib as another CETP inhibitor lost to the gap between lipid improvement and clinical benefit (Bratisl Lek Listy 2016)
Original title: Unending saga of fighting cholesterol: Evacetrapib is another fallen warrior
Despite the enormous success of statins and modern antihypertensive drugs in reducing cardiovascular morbidity and mortality, these therapies remain incompletely effective, sustaining interest in other molecular dyslipidemia targets. This commentary marks the decades-long, expensive trial program for the CETP inhibitor evacetrapib as coming to a crash landing in April 2016: despite dramatic improvement in HDL cholesterol and decline in LDL cholesterol, its cardiovascular disease outcome was comparable to placebo. The author notes that this failure in the CETP molecular target field leaves the PCSK9 inhibitor field as a potential alternative path to identifying a molecular target that normalizes dyslipidemia without harming physiologically essential lipids.
Original abstract
Despite an enormous success in reducing morbidity and mortality in cardiovascular disease (CVD), statins and modern antihypertensive medications are not universally effective. Research has focused on potential molecular targets in dyslipidemia. Decades-long, expensive trial with CETP (cholesterylester transfer protein) inhibitor evacetrapib, came in April 2016 to crash landing. Despite dramatic improvement in "good" HDL-cholesterol and decline in "bad" LDL-C, the effect of evacetrapib in CVD patients was comparable to placebo. Notwithstanding failure in this molecular target field, results with another agent the PCSK9 inhibitor, may identify the molecular site that would normalize dyslipidemia, without harming physiologically essential lipids (Fig. 2, Ref. 19).
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.